Effects of caloric restriction on O-GlcNAcylation, Ca2+ signaling, and learning impairment in the hippocampus of ob/ob mice

Publication date: August 2016
Source:Neurobiology of Aging, Volume 44
Author(s): Byeong Tak Jeon, Rok Won Heo, Eun Ae Jeong, Chin-ok Yi, Jong Youl Lee, Kyung Eun Kim, Hwajin Kim, Gu Seob Roh
Diabetes may adversely affect cognitive function and, conversely, caloric restriction (CR) increases longevity and improves memory. To shed light on the unknown underlying mechanisms involved in these observations, we examined the effects of CR on serum metabolic parameters and hippocampal protein expression in the ob/ob mice model of obesity-induced diabetes. We found that CR reduced hepatic steatosis and insulin resistance in ob/ob mice. In addition, CR increased the levels of hippocampal O-linked-N-acetylglucosamine (O-GlcNAc) and GlcNAc transferase and decreased the expression of calcium/calmodulin–dependent protein kinase II, lipocalin-2, and phosphorylated tau. Furthermore, CR lessened the learning deficits that are typically seen in ob/ob mice. These findings indicate that CR may reverse obesity-related brain glucose impairment and intracellular Ca²⁺ dysfunction and relieve learning impairment associated with diabetes.



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